The document summarizes the process of beta-oxidation of fatty acids. It occurs in the mitochondrial matrix in four steps - oxidation, hydration, oxidation, and cleavage - resulting in the sequential removal of two-carbon acetyl-CoA units. Fatty acids are first activated to acyl-CoAs in the cytosol then transported into the mitochondria by the carnitine shuttle system to undergo beta-oxidation, generating acetyl-CoA, NADH, and FADH2. Defects in this process can cause various metabolic disorders like fatty acid oxidation disorders.
This Medicoapps Masterclass discusses about Cori cycle. Various Topics Discussed are given below
Cori cycle Various Steps
Significance of Cori’s Cycle
Exam points of Cori’s Cylce
The citric acid cycle, also known as the tricarboxylic acid cycle (TCA cycle) or the Krebs cycle—is a series of chemical reactions used by all aerobic organisms to generate energy through the oxidation of acetate—derived from carbohydrates, fats, and proteins—into carbon dioxide.
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
This Medicoapps Masterclass discusses about Cori cycle. Various Topics Discussed are given below
Cori cycle Various Steps
Significance of Cori’s Cycle
Exam points of Cori’s Cylce
The citric acid cycle, also known as the tricarboxylic acid cycle (TCA cycle) or the Krebs cycle—is a series of chemical reactions used by all aerobic organisms to generate energy through the oxidation of acetate—derived from carbohydrates, fats, and proteins—into carbon dioxide.
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
explains the palmitate synthesis- which is most common FA stored in Adipose tissue , elongation system and Desaturation system, compares oxidation with synthesis.
For this assignment, we were instructed to create a powerpoint presentation of at least 12 slides that adequately covered an academic subject of our choice. All sources for media is cited in the work cited at the end of the presentation.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
2. Beta-Oxidation may be defined as the
oxidation of fatty acids on the β-carbon atom.
This results in the sequential removal of a two
carbon fragment, acetyl CoA.
3. Three stages
Activation of fatty acids - in the cytosol
Transport of fatty acids into mitochondria
Beta-Oxidation proper in the mitochondrial
matrix
Fatty acids are oxidized by most of the
tissues in the body.
Brain, erythrocytes & adrenal medulla cannot
utilize fatty acids for energy requirement.
4. Fatty acid activation taking place in cytoplasm.
Fatty acids are activated to acyl CoA by
thiokinases or acyl CoA synthetases.
The reaction occurs in two steps & requires
ATP, coenzyme A and Mg2+
Fatty acid reacts with ATP to form
acyladenylate which then combines with
coenzyme A to produce acyl CoA.
5. Two high energy phosphates are utilized,
since ATP is converted to pyrophosphate (PPi).
The enzyme inorganic pyrophosphatase
hydrolyses PPi to phosphate.
The immediate elimination of PPi makes this
reaction totally irreversible.
6. Three different enzymes, one each for short
chain, medium chain & long chain fatty acids.
Small chain fatty acids may also be activated
by thiophorase enzyme, using succinyl CoA.
8. The inner mitochondrial membrane is
impermeable to fatty acids.
A specialized carnitine carrier system (carnitine
shuttle) operates to transport activated fatty
acids from cytosol to the mitochondria.
Carnitine is β-hydroxy γ-trimethyl
aminobutyrate, synthesized by lysine &
methionine in liver & kidney.
9. o It occur in four stages.
1. Acyl group of acyl CoA is transferred to
carnitine catalyzed by carnitine
acyltransferase I (CAT-I) (present on the outer
surface of inner mitochondrial membrane).
2. The acyl-carnitine is transported across the
membrane to mitochondrial matrix by a
specific carrier protein (Translocase).
10. 3. Carnitine acyltransferase ll (CAT-II) (found on
the inner surface of inner mitochondrial
membrane) converts acyl-carnitine to acyl
CoA.
4. The carnitine released returns to cytosol for
reuse by translocase.
12. Each cycle of β –oxidation, liberating a two
carbon unit-acetyl CoA, occurs in a sequence
of four reactions
1. Oxidation
2. Hydration
3. Oxidation
4. Cleavage
13. Acyl CoA undergoes dehydrogenation by an
FAD-dependent flavoenzyme, acyl CoA
dehydrogenase.
A double bond is formed between α & β carbons
(i.e., 2 & 3 carbons)
2. Hydration:
Enoyl CoA hydratase brings about the hydration
of the double bond to form β -hydroxyacyl CoA.
14. 3. Oxidation
β-Hydroxyacyl CoA dehydrogenase
catalyses the second oxidation & generates NADH.
The product formed is β-ketoacyl CoA.
4. Cleavage
The final reaction in β -oxidation is the liberation of
a 2 carbon fragment, acetyl CoA from acyl CoA.
This occurs by a thiolytic cleavage catalysed by β-
ketoacyl CoA thiolase (or thiolase).
15. The new acyl CoA, containing two carbons
less than the original, reenters the β-
oxidation cycle.
The process continues till the fatty acid is
completely oxidized.
16. R – CH2 – CH2 – CH2 – C – O-
Fatty acid
O
R – CH2 – CH2 – CH2 – C –
Acyl CoA
O
Thiokinase
ATP
ADP + PPi
Mg+2
SCoA
Carnitine Transport system
Cytosol
Mitochondria
CoASH
β-Oxidation of fatty acids
17. R – CH2 – CH2 – CH2 – C – SCoA
Acyl CoA
O
FAD
FADH22ATP ----- ETC
Acyl CoA
Dehydrogenase
R – CH2 – CH2 CH2 – C – SCoA
Trans-enoyl CoA
O
R – CH2 – CH – CH2 – C – SCoA
β - Hydroxyacyl CoA
OOH
Enoyl CoA
Hydratase
H2O
SIDS
OH
18. R – CH2 – CH – CH2 – C – SCoA
β - Hydroxyacyl CoA
OOH
NAD+
NADH + H+3ATP ----- ETC
β-Hydroxy Acyl CoA
Dehydrogenase
R – CH2 – C – CH2 – C – SCoA
β - Ketoacyl CoA
OO
Thiolase
R – CH2 – C – SCoA
Acyl CoA
O
CH3 – C – SCoA
Acetyl CoA
O
TCA
Cycle
Acyl CoA
CoASH
19. Palmitoyl CoA + 7 CoASH + 7 FAD +
7 NAD+ + 7 H2O 8 Acetyl CoA + 7
FADH2 +7 NADH + 7H+
Palmitoyl CoA undergoes 7 cycles of β -
oxidation to yield 8 acetyl CoA.
Acetyl CoA can enter citric acid cycle & get
completely oxidized to CO2 & H2O.
20. Mechanism ATP yield
I. β- 0xidation 7 cycles
7 FADH2 [Oxidized by Electron Transport Chain (ETC) each
FADH2 gives 2 ATP ]
7 NADH (Oxidized by ETC, each NADH
Liberate 3ATP)
14
21
II. From 8 Acetyl CoA
Oxidized by citric acid cycle, each acetyl CoA
provides 12 ATP
96
Total energy from one molecule of palmitoyl CoA
Energy utilized for activation
(Formation of palmitoyl Co A)
131
-2
Net yield of oxidation of one molecule of palmitate =129
21. The availability of free fatty acid (FFA)
regulates the net utilisation through β-
oxidation.
The level of FFA is controlled by
glucagon:insulin ratio.
Glucagon increases FFA level & insulin has
the opposite effect.
22. CAT-I is the regulator of entry of fatty acid
into mitochondria.
Malonyl CoA inhibits CAT-I activity.
Thus during de novo synthesis of fatty acid,
the beta oxidation is inhibited.
23. Unexpected death of healthy infants, usually
overnight
Due to deficiency of medium chain acyl CoA
dehydrogenase.
Glucose is the principal source of energy, soon
after eating or feeding babies.
24. After a few hours, the glucose level & its
utilization decrease & the rate of fatty acid
oxidation must simultaneously increase to
meet the energy needs.
The sudden death in infants is due to a
blockade in β -oxidation caused by a
deficiency in medium chain acyl CoA
dehydrogenase (MCAD)
25. Characterized by severe hypoglycemia,
vomiting, convulsions, coma & death.
lt is caused by eating unriped ackee fruit-
contains an unusual toxic amino acid,
hypoglycin A.
This inhibits the enzyme acyl CoA
dehydrogenase & β -oxidation of fatty acids is
blocked, leading to various complications
26. Abnormalities in transport of fatty acids into
mitochondria & defects in oxidation leads to
deficient energy production by oxidation of long
chain fatty acids.
Features:
Hypoglycemia, hyperammonemia, weakness &
liver diseases.
Acyl carnitine accumulates when the transferases
or translocase is deficient.
Dietary supplementation of carnitine improve the
condition.
27. Oxidation of odd chain fatty acids is similar
to that of even chain fatty acids.
At the end 3 carbon unit, propionyl CoA is
produced.
Propionyl CoA is converted into succinyl CoA.
Succinyl CoA is an intermediate in TCA cycle
Propionyl CoA is gluconeogenic.
28. Propionyl CoA is carboxylated to D-methyl
malonyl CoA by a biotin dependent
carboxylase.
Biotin & ATP is utilized in this step.
Methylmelonyl CoA Recemase:
Recemase acts upon D-methyl malonyl CoA to
give L-methyl malonyl CoA.
This reaction is essential for the entry of this
compound into metabolic reactions of body.
29. Methylmalonyl CoA Mutase:
Mutase catalyzes the conversion of L-methyl
malonyl CoA (a branched chain compound) to
succinyl CoA (a straight chain compound).
Mutase is an vitamin B12 dependent enzyme.
Succinyl CoA enters the TCA cycle, & converted
into oxaloacetate, it is used for
gluconeogenesis.
Propionyl CoA is also derived from
metabolism of valine & isoleucine.
30. CH3
I
CH2
I
CO-S-CoA
Propionyl CoA
CH3
I
H - C- COO-
I
CO-S-CoA
D-methyl malonyl CoA
CH3
I
-OOC – C - H
I
CO-S-CoA
L - methyl malonyl CoA
COO-
I
CH2
I
CH2
I
CO-S-CoA
Succinyl CoA
Propionyl CoA
carboxylase
ATP ADP + Pi
CO2
Methylmalonyl
CoA recemase
Methylmalonyl
CoA mutase
Vitamin B12
TCA
Biotin
31. Propionyl CoA carboxylase deficiency:
Characterized by propionic acidemia,
ketoacidosis & developmental abnormalities.
Methyl malonic aciduria:
Two types of methyl malonic acidemias
Due to deficiency of vitamin B12
Due to defect in the enzyme methyl malonyl
CoA mutase or recemase.
32. Accumulation of methyl malonic acid in body.
Methyl malonic acid is excreted into urine.
Symptoms:
Severe metabolic acidosis, damages the
central nervous system & growth retardation.
Fatal in early years of life.
Treatment:
Some patients respond to treatment with
pharmacological doses of B12.
33. Oxidation of fatty acids on α-carbon atom is
known as α-oxidation.
In this, removal of one carbon unit from the
carboxyl end.
Energy is not produced.
No need of fatty acid activation & coenzyme A
Hydroxylation occurs at α-carbon atom.
34. It is then oxidized to α-keto acid.
This, keto acid undergoes decarboxylation,
yielding a molecule of CO2 & FA with one
carbon atom less.
Occurs in endoplasmic reticulum.
Some FA undergo α - oxidation in
peroxisomes.
35. α- oxidation is mainly used for fatty acids
that have a methyl group at the beta-carbon,
which blocks beta- oxidation.
Major dietary methylated fatty acid is
phytanic acid.
It is derived from phytol present in
chlorophyll, milk & animal fats.
36. Due to deficiency of the enzyme α-
hydroxylase (phytanic acid oxidase)
α – oxidation does not occur.
Phytanic acid does not converted into
compound that can be degraded by beta –
oxidation.
Phytanic acid accumulates in tissues.
37. Severe neurological symptoms,
polyneuropathy, retinitis pigmentosa, nerve
deafness & cerebellar ataxia.
Restricted dietary intake of phytanic acid
(including milk-is a good source of phytanic
acid)
38. Minor pathway, takes place in microsomes.
Catalyzed by hydroxylase enzymes involving
NADPH & cytochrome P-450.
Methyl (CH3) group is hydroxylated to CH2OH &
subsequently oxidized with the help of NAD+ to
COOH group to produce dicarboxylic acids.
When β-oxidation is defective & dicarboxylic acids
are excreted in urine causing dicarboxylic aciduria.
39. It is a rare disorder.
It is characterized by absence of
peroxisomes in almost all the tissues.
Long chain fatty acids are not oxidized.
Long chain fatty acids are accumulated in
tissues-mainly brain, liver & kidney.
It also known as cerebrohepatorenal
syndrome.
40. Textbook of Biochemistry-U Satyanarayana
Textbook of Biochemistry-DM Vasudevan